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Anti-Inflammatory Responses Complement regulatory proteins: e.g. C1 inhibitor, C4 binding protein, Factor H, Factor I, complement receptor CR1, decay accelerating factor. Acute phase proteins e.g. protease inhibitors, ceruloplasmin. PGE 2, TGF , Prostaglandins IL-10 sIL-1R
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Immunopathology Virus-bacterium synergistic pathology Sepsis and Endotoxemia Molecular mimicry Superantigens
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Virus-Bacterium Synergy Enhancement of inflammatory response by bacterial growth, IFN , complement. Increased tissue damage by bacterial toxins (cytolysin, LPS) Amplification of macrophage reactivity by cytokines, LPS,
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Sepsis and Endotoxemia Proinflammatory cytokines: TNF , IFN , IL-1, IL-6, IL-8, IFN , IFN C5a Neutropenia Soluble cytokine receptors (TNF-R, IL-1R)
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Molecular Mimicry Chlamydia - heart Campylobacter - Guillan-Barre’ syndrome
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Superantigens S. aureus enterotoxins causing food poisoning, vomiting & diarrhea (SEA, SEB). Lymphocyte proliferation Cytokine production Toxic shock syndrome.
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Immune Evasion Camouflage Encapsulation Antigenic mimicry Antigenic masking Antigenic shift Latency Intracellular replication Subversion Production of anti-Ig proteases Destruction of phagocyte Inhibition of chemotaxis Inhibition of phagocytosis Inhibition of phagolysosome fusion Resistance to lysosomal enzymes Superantigens
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Mechanisms of Immune Evasion I: Camouflage Capsule formation S aureus protein A Sialic acid LPS O protein S aureus coagulase M bacterium granuloma formation
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Mechanisms of Immune Evasion III: Anti-Phagocytosis Inhibit opsonization (S aureus protein A) Inhibit chemotaxis Kill phagocyte (S aureus streptolysin) Inhibit phagocytosis (S pneumoniae capsule, S pyogenes M protein) Inhibit lysosomal fusion (M. tuberculosis) Escape lysosome and grow in cytoplasm (Mycobacteria, Salmonella, S. aureus) Block activation by IFN (Mycobacteria) Viral envelope glycoproteins LPS
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Mechanisms of Immune Evasion II: Proteases Inhibit opsonization (N gonorrhoeae IgA protease) Inhibit chemotaxis Kill phagocyte (S aureus streptolysin) Inhibit phagocytosis (S pneumoniae capsule, S pyogenes M protein) Inhibit lysosomal fusion (M. tuberculosis) Escape lysosome and grow in cytoplasm (Mycobacteria, Salmonella, S. aureus) Block activation by IFN (Mycobacteria) Viral envelope glycoproteins LPS
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Viral Mechanisms of Immune Evasion I Humoral Response >Latency e.g. HSV, retroviruses >Syncytia formation e.g. HSV, VZV, HIV >Antigenic variation e.g. HIV >Blocking antigen e.g. HBV e Ag >Complement decay e.g. HSV
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Viral Mechanisms of Immune Evasion II. Interferon >HBV blocks transcription of IFN >EBV synthesizes BRC1, an analogue of IL-10. >Adenovirus RNA - double stranded duplex blocks interferon antiviral action; early protein binds cl I heavy chain preventing upregulated expression
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Viral Mechanisms of Immune Evasion III Immune Cell Function >CTL cytolysis e.g. HSV >T H depletion e.g. HIV >Immunosuppression e.g. measles, EBV
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Viral Mechanisms of Immune Evasion IV. Antigen Presentation >Inhibition of Cl I MHC expression e.g. Adenovirus, CMV >Inactivating peptides e.g. HBV Inhibition of Inflammation >Blocking of inflammatory cytokines e.g. Poxviruses, adenovirus.
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Infection and Pathogenesis Colonization (Benign or asymptomatic) Infection Disease (Pathogenesis) Clinical or Subclinical
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Requisites for Successful Growth Attachment Nutrition Survival from host defence Transmission
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Virulence Factors Factors which promote infection and which contribute to disease Studied with mutants Are multifactorial Consist of: >Factors promoting colonization and invasion >Factors which are pathogenic
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Bacterial Virulence Factors I: Colonization Adherence: Capsules, Pili, adhesins Penetration: e.g. invasins Host gene modification.
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Capsules Present in some gram negative and positive bacteria. May be composed of protein or polysaccharide layers. Is poorly antigenic and anti-phagocytic Can act as a barrier to toxic hydrophobic molecules such as detergents. Can promote adherence to other bacteria or cell surfaces
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Pili (Fimbriae) Composed of subunits of pilin. Promote adherence to other bacteria or host. Synonyms: adhesins, lectins, evasins, aggressins. Fragile, often replaced.
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Bacterial Pathogenesis Toxic byproducts of bacterial growth e.g. acids, gas, proteases Toxins >Endotoxins e.g. LPS >Exotoxins Immunopathogenesis e.g. Chlamydia, treponemes (syphilis), Borrelia (Lyme disease)
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Endotoxins: Lipopolysaccharide Fever Leukopenia, followed by leukocytosis Complement activation Thrombocytopenia Coagulation Decreased blood circulation Shock Death
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Exotoxins AB. e.g. Shigella dysenteriae, C. tetani, V. cholerae. Cell Membrane Disruption. e.g. C. perfringens Superantigens. e.g. S. aureus
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Exotoxins I: AB (i)
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Exotoxins I:AB (ii)
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Exotoxins I: AB (iii)
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